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Abstract

F.A. Shiekh¹, V.M. Miller³ and J.C. Lieske¹,²

¹Departments of Internal Medicine, ²Laboratory Medicine and Pathology and ³Surgery, Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA
Although much has been learned regarding the pathogenesis of kidney stones, the reason(s) why some individuals form stones while others do not remains incompletely understood. Nanoparticles, which have been observed in geologic samples, have also been isolated from biologic specimens, including kidney stones. These nanoparticles have certain properties that are consistent with a novel life form, including in vitro self-replication, and contain lipids, DNA and proteins. Therefore, it has been hypothesized that nanoparticles may represent a type of infective agent that initiates stone formation in some individuals. Despite a large body of intriguing and suggestive evidence, the true biologic nature of these entities has been elusive, and controversy remains as to whether these nano-sized particles are analogous to other recently described unusual and novel microorganisms, or a transmissible, yet inert nanoparticle. Although unique DNA or RNA has yet to be identified, a proteomic biosignature is beginning to emerge that may allow more definitive clinical investigation. This review evaluates the current evidence regarding nanoparticles as causal to disease and emphasizes the need for additional research to further elucidate their role in human stone formation.Correspondence to:
J.C. Lieske, MD; Mayo Clinic Division of Nephrology and Hypertension, 200 1st Street SW, Rochester, MN 55905, USA
Email: lieske.john@mayo.edu

Abstract

R. Masai¹, H. Wakui¹, M. Togashi¹, N. Maki¹, H. Ohtani², A. Komatsuda¹ and K. Sawada¹

¹Third Department of Internal Medicine, Akita University School of Medicine and ²Department of Nephrology and Dialysis, Akita Kumiai General Hospital, Akita, Japan
Background: There are three subtypes of monoclonal immunoglobulin deposition disease: light chain deposition disease (LCDD), light and heavy chain deposition disease (LHCDD), and heavy chain deposition disease (HCDD). Although it has been considered that LHCDD is a variant of LCDD, information on clinicopathological features and prognosis in LHCDD is presently limited. Methods: We reviewed 5,443 renal biopsies, and evaluated clinicopathological features and outcomes in patients with LHCDD, in comparison with those in patients with LCDD and previously reported patients with HCDD. We also characterized paraprotein deposits in patients with LHCDD. Results: We identified 6 patients with LHCDD, 6 patients with LCDD, and 1 patient with HCDD. The most common clinicopathological findings in patients with LHCDD were proteinuria, renal insufficiency, and nodular sclerosing glomerulopathy. Three patients had IgG-k deposits and 3 patients had IgG-l deposits. Heavy chain subclass analysis performed in 4 patients showed IgG3 deposits in all patients. Dual immunostaining revealed glomerular colocalization of light and heavy chains. In contrast with LCDD, glomerular C3 and C1q deposits were common findings in LHCDD and HCDD. All patients with LHCDD were treated with steroids and cytotoxic agents, but no effect on proteinuria was observed. Three patients developed end-stage renal disease requiring hemodialysis. The underlying hematological disorders in LHCDD and HCDD were milder than in LCDD. Early renal survival and overall patient survival in our patients appeared to be better in LHCDD than in LCDD. Conclusions: There are apparent differences in clinicopathological features and prognosis between LHCDD and LCDD. LHCDD is probably more similar to HCDD.Correspondence to:
H. Wakui, MD; Third Department of Internal Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita City, Akita 010-8543, Japan
Email: wakui@med.akita-u.ac.jp

Abstract

V. Lezaic¹, B. Tirmenstajn-Jankovic⁵, D. Bukvic⁶, B. Vujisic², M. Perovic³, N. Novakovic⁴, V. Dopsaj⁴, I. Maric⁶ and Lj. Djukanovic¹

Departments of ¹Nephrology, ²Cardiology, ³Radiology and ⁴Biochemical Laboratory, Clinical Center Beograd, ⁵Medical Center Zajecar and ⁶Institute of Endemic Nephropathy, Lazarevac, Serbia
Background and aims: Chronic kidney disease mineral- and bone disorder (CKD-MBD) has been studied more often in dialysis than in predialysis CKD patients. The association between efficacy of hyperphosphatemia control and chronic renal failure (CRF) progression, prevalence of bone disease and cardiovascular calcification was the objective of the present investigation. Material and methods: 42 patients with CKD in Stage 5, regularly monitored for 5 years, were divided into Group 1 of 20 patients with normal serum phosphate (sPO₄) levels and Group 2 of 22 patients with hyperphosphatemia registered at the majority of checks. Serum urea, creatinine, calcium (sCa) and sPO₄ levels were regularly determined in the retrospective 5-year period. At the end of this period iPTH, bone alkaline phosphatase-BAP and inflammation markers (CRP, fetuin-A) were measured, valvular and arterial calcifications were detected by B mode echocardiogram and soft-tissue native radiograms of the pelvis and the wrist. Results: Progression of CRF (1/sCr over time) was faster in Group 2 than in Group 1 (b = –0.0577 vs. –0.0288, p = 0.003) during the study period. Average BAP and iPTH values were similar in both groups and 23/42 patients had PTH > 300 pg/ml. Arterial and valvular calcifications were found in 5/23 patients from Group 1 and 14/22 patients from Group 2 (p = 0.011). Linear regression analysis revealed sPO₄ as a predictor for total calcification number, inflammatory diseases as a predictor for valvular calcifications, while sPO₄ and iPTH were predictors for arterial calcifications. Conclusions: More than half the patients with Stage 5 CKD not yet on dialysis exhibited elevated PTH. Faster CRF progression and frequent arterial and valvular calcifications were seen in patients with poor phosphate control and sPO₄ was selected as an independent predictor of total calcification score.Correspondence to:
V. Lezaic, MD, PhD; Department of Nephrology, Clinical Center of Serbia, Pasterova 2, 11000 Beograd, Serbia
Email: visnjal@eunet.yu

Abstract

M. Cetin¹, E. Ucar², O. Guven³ and S. Ocak⁴

¹Department of Microbiology and Clinical Microbiology, University Faculty of Medicine, ²Department of Internal Medicine, ³Department of Urology and ⁴Department of Infection Disease, Hatay, Turkey
In this study, we compared the distribution and antibiotic susceptibility patterns of bacterial strains isolated from patients with community-acquired urinary tract infections in Southern Turkey, Hatay, during 2004 and 2005. The majority (82.3%) of the isolates were from women while the remaining (17.7%) were from men. Of all samples tested, 49% were culture-positive with a bacterial pathogen. The most frequently isolated bacterial species were Escherichia coli (45.1%), coagulase-negative Staphylococcus (CNS) (15.5%) and Klebsiella spp. (10.9%). E. coli was more prevalent in women (p < 0.05) while Klebsiella spp., Proteus spp. and Pseudomonas spp. were found more prevalent in men (p < 0.05). Increasing resistance to gentamicin, amikacin and cefazolin, and decreased resistance to ciprofloxacin, ofloxacin, levofloxacin and cotrimoxazole were observed in E. coli isolates over the 2 years. While the lowest resistance rates for E. coli occurred in 2004 (26.0%) and 2005 (20.5%) for cefuroxime, the highest resistance rates occurred in 2004 (81.3 and 47.9%) and 2005 (61.3 and 49.6%) for ampicillin and amoxicillin-clavulanate, respectively. The results of this study stress that antibiotic usage policies, especially empirical therapies, should be based on antimicrobial resistance surveillance studies.Correspondence to:
E. Ucar, MD; Mustafa Kemal Universitesi Tip Fakültesi, Hastaliklari ABD, 31100 Hatay, Turkey
Email: edip_ucar@yahoo.com

Abstract

N. Kamar¹,⁵*, A. Huart¹*, I. Tack², L. Alric³, J. Izopet⁴,⁶ and L. Rostaing¹,⁶

¹Nephrology, Dialysis and Multiorgan Transplant Unit, CHU Rangueil, ²Renal Functional Explorations Unit CHU, Rangueil, ³Department of Hepatology, CHU Purpan, ⁴Laboratory of Virology, CHU Purpan, ⁵INSERM U ⁸⁵⁸ Toulouse and ⁶INSERM U ⁵⁶³, Toulouse, France
Aims: The purpose of this study was to evaluate the renal side-effects of adefovir therapy in kidney-transplant (KT) recipients with chronic hepatitis B virus (HBV) infection, who have become resistant to lamivudine therapy. Patients and methods: 11 kidney-transplant (KT) patients (10 men, 1 woman, median age 54 (46 – 67) years) had lamivudine-resistant chronic HBV infection. With respect to HBV markers, all were HBs Ag-positive, 8 were HBe Ag-negative/HBe antibody- (Ab) positive, i.e. precore mutant, and 3 were HBe Ag-positive/HBe Ab-negative. They were all given adefovir at 10 mg/d (3 cases) or 5 mg/d (6 cases) or 2.5 mg/d (2 cases) according to creatinine clearance. Results: Compared to baseline without adefovir therapy, at last follow-up, adefovir therapy was associated, at 1 and 2 years post therapy, with a significant decrease in aspartate (AST) (28 (17 – 53), 28 (10 – 79) vs. 58 (24 – 1,282) IU/l, p = 0.001), alanine (ALT) (38 (13 – 55), 36 (17 – 92) vs. 72 (31 – 1,594) IU/l, p = 0.0032] aminotransferase levels, and gammaGT (31 (14 – 51), 25 (14 – 196) vs. 44 (25 – 742) IU/l, p = 0.03). With respect to HBV DNA, when compared to baseline, there was a significant decrease at both years 1 and 2 post therapy (p = 0.01). With respect to KT function at 2 years after starting adefovir, there was a significant increase in serum creatinine from 125 (± 35) to 141 (± 32) µmol/l, (p = 0.02) and a significant increase in 24-h proteinuria. With respect to renal tubular parameters, as compared to baseline without adefovir therapy, one year after adefovir therapy was commenced there was a significant decrease in urinary pH from 6.6 (+0.6) to 5.65 (± 0.7); p = 0.03, a significant decrease in bicarbonaturia (from 0.33 ± 0.7 to 0.1 ± 0.3 mmol/h, p = 0.01), an increase in urinary excretion of H⁺ (1.79 (± 1.33) to 2.44 (± 1.18) mmol/l (p = 0.03)), a significant decrease in phosphatemia (0.82 ± 0.19 vs. 0.65 ± 0.13 mmol/l, p = 0.04) and a significant decrease in phosphaturia threshold, a significant decrease in tubular phosphorus reabsorption (75.5 ± 9.4% vs. 61.8 ± 16%, p = 0.05), and a significant increase in the phosphorus index of excretion (0.18 ± 0.114 vs. 0.35 ± 0.164, p = 0.01). Conclusion: We have demonstrated that low-dosage adefovir therapy in kidney-transplant patients is relatively safe as far as renal parameters are concerned, even though we observed a slight impairment of renal proximal-tubular function.Correspondence to:
Prof. L. Rostaing; CHU Rangueil, Service de Néphrologie, Transplantation d’Organes, Hémodialyse, 1 av. Jean Poulhès, TSA 50032, 31059 Toulouse Cedex 9, France
Email: rostaing.l@chu-toulouse.fr

Abstract

D. Maoz¹, R. Reinitz¹,³, U. Rimon², A. Knecht³, L. Badayev³, E. Holtzman³ and J. Schneiderman¹

¹Department of Vascular Surgery, ²Interventional Radiology, ³Nephrology, Sackler Faculty of Medicine, Sheba Medical Center, Tel Hashomer, Tel Aviv University, Tel Aviv, Israel
Background: Hemodialysis arteriovenous graft (AVG) patency is dependent on favorable flow characteristics. We examined hemodynamic, humoral risk factors, and the effects of stringent flow surveillance coupled with prompt corrective intervention on long-term graft patency. Methods: Over a 29-month period 92 chronic hemodialysis patients with AVG were evaluated monthly by flow surveillance. Clinical diagnosis of failing graft, which promoted angiography and corrective intervention was based on flow reduction, and patient’s unique medical history and hemodynamic parameters. Results: Graft arteriography revealed stenotic lesions in 94.5% of the cases, necessitating endovascular or surgical angioplasty. Low ejection fraction, early postoperative intervention, and low baseline flow were associated with a statistically significant reduction in intervention-free interval (p < 0.05). Mean AVG flow threshold prior to intervention was 463 ± 154 ml/min, corresponding to a mean flow reduction of 45 ± 12%. Total graft thrombosis rate was 0.21 thrombotic episodes/patient year. Primary graft patency at 6, 12, and 24 months was 76, 44 and 35%, and secondary patency 99, 97, 88%, respectively. Conclusions: Stringent flow surveillance policy coupled with prompt intervention has been proven effective in maintaining AVG long-term patency. Patients with decreased ejection fraction, early post-operative intervention, and low baseline AVG flow are prone to graft thrombosis.Correspondence to:
J. Schneiderman, MD;Department of Vascular Surgery, Sheba Medical Center, Tel Hashomer, 52621, Israel
Email: jschneid@netvision.net.il

Abstract

T. Köhnlein¹, A. Schmidt¹, M. Moesenthin², J. Dierkes³, K.H. Neumann² and T. Welte¹

¹Department of Respiratory Medicine, Hannover Medical School, Hannover, ²Division of Nephrology, Otto-von-Guericke Universität Magdeburg and ³Institute of Clinical Chemistry, Otto-von-Guericke Universität Magdeburg, Germany
Background: Increased cardiac troponin T (cTnT) and C-reactive protein (CRP) levels predict mortality in patients with end-stage renal disease (ESRD) on maintenance hemodialysis. Obstructive sleep apnea (OSA) is associated with severe cardiac stress and systemic inflammation. We hypothesized that in patients with ESRD elevated levels of cTnT and CRP are consequences of unrecognized OSA. Methods: After diagnostic polysomnography, serum levels of cTnT and CRP were assessed in two groups of patients. The first group with normal renal function which served as a control group, was recruited from routine patient referrals to the sleep laboratory at the University Hospital Magdeburg. The second group consisted of patients with ESRD on thrice-weekly maintenance hemodialysis treatment (hemodialysis group). Results: After screening, 15 patients in each group were eligible for inclusion. OSA (apnea hypopnea index (AHI) >= 10) was associated with significantly elevated serum CRP levels of 5.1 ± 4.9 mg/l in the control group and 11.6 ± 10.2 mg/l in the hemodialysis group, compared with patients in the respective groups without OSA. In the control group, cTnT levels were below the lower detection limit, independent of OSA severity. Patients with ESRD but without OSA had low cTnT levels, similar to those of patients in the control group (0.014 ± 0.01 ìg/l), whereas patients with ESRD and OSA had significantly elevated serum cTnT levels (0.38 ± 0.3 µg/l, p < 0.05). Conclusions: OSA is associated with higher CRP levels in patients with normal or impaired renal function, but cTnT is elevated in OSA patients with impaired renal function only. In this pilot study, both parameters suggest an important role of sleep related breathing disorders on cardiac stress and chronic inflammation.Correspondence to:
Dr. T. Köhnlein; Hannover Medical School, Department of Respiratory Medicine, Carl-Neuberg-Straße 1, 30625 Hannover, Germany
Email: koehnlein.thomas@mh-hannover.de

Abstract

S.D. Navaneethan¹, J. Taylor², B. Goldman³ and A. Bose²

¹Department of Nephrology and Hypertension, Cleveland Clinic, Cleveland OH, ²Division of Nephrology and ³Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine, Rochester, NY, USA
Membranous glomerulonephritis and minimal change disease are the most common forms of glomerular diseases noted in patients with graft versus host disease after hematopoietic stem cell transplantation. Herein, we report a patient who developed anti-neutrophil cytoplasmic antibody associated crescentic IgA nephropathy within 3 months after autologous hematopoietic stem cell transplantation. He was treated with intravenous pulse steroids and monthly intravenous cyclophosphamide for 6 months followed by cyclophosphamide every 3 months and tapering dose of steroids. His proteinuria resolved and renal function remained stable. Two cases of crescentic IgA nephropathy have been reported in patients who underwent allogenic hematopoietic stem cell transplantation. The etiology of IgA nephropathy developing after hematopoietic stem cell transplantation is unclear and larger registry-based studies are needed to further explore this condition.Correspondence to:
S.D Navaneethan, MD, MPH; Department of Nephrology and Hypertension, Cleveland Clinic, 9500 Euclid Avenue A -51, Cleveland, OH 44195, USA
Email: navanes@ccf.org

Abstract

S. Nunez¹,², K.N. Konstantinov¹,², K.S. Servilla²,³, M.F. Hartshorne⁴, W.L. Williams⁵, L.J. Gibel⁶ and A.H. Tzamaloukas²,³

¹Rheumatology Section, New Mexico Veterans Affairs Health Care System (VAHCS), ²Department of Medicine, University of New Mexico (UNM) School of Medicine, ³Nephrology Section, New Mexico VAHCS, ⁴Radiology Service, New Mexico VAHCS and Department of Radiology, UNM, ⁵Pathology Service, New Mexico VAHCS and Department of Pathology, UNM, and ⁶Urology Section, New Mexico VAHCS and Department of Surgery UNM School of Medicine, Albuquerque, NM, USA
We report a patient with scleroderma, renal cell carcinoma (RCC) and membranous nephropathy (MN). Certain clinical and laboratory features suggested that RCC caused or enhanced the other two conditions. A 55-year-old man developed scleroderma which progressed rapidly during its first 2 years with development of hypertension and acute renal failure, peak serum creatinine (SCr) 327 µmol/l (3.7 mg/dl) and partial improvement of the renal function (SCr 239 µmol/l or 2.7 mg/dl) after initiation of an angiotensin converting enzyme inhibitor. He subsequently developed nephrotic syndrome (urine protein excretion 9 gm/24-h) and progressive renal failure, with SCr 469 ± 18 µmol/l (5.3 ± 0.2 mg/dl). An anti-nuclear mitotic apparatus protein (NUMA) antibody, which is uncommon in scleroderma but has been linked to certain malignancies, was found in his serum. A left upper pole RCC was removed by heminephrectomy. MN was found in the renal parenchyma adjacent to the excised tumor. In the 3.5 years following surgery, the clinical manifestations of scleroderma have been arrested while the medications prescribed for this condition have been greatly reduced. Proteinuria is consistently less than 1 gm/24-h and 42 months after surgery serum creatinine was 256 µmol/l (2.9 mg/dl). Nutrition has also improved. Although this case may represent chance occurrence of three uncommon diseases (scleroderma, RCC, MN) in the same individual, the sustained improvement of the manifestations of scleroderma and MN after resection of the RCC contrasted to the rapid course of these conditions until the surgery, and the presence in the patient’s serum of an autoantibody which is uncommon in patients with scleroderma, but has been linked to malignancy, suggest a pathogenetic relationship between the three conditions.Correspondence to:
A.H. Tzamaloukas, MD; New Mexico VA Health Care System (111C), 1501 San Pedro, SE, Albuquerque, NM 87108, USA
Email: Antonios.Tzamaloukas@med.va.gov

Abstract

Y. Huan, J.E. Tomaszewski and D.L. Cohen

Renal and Pathology Divisions, University of Pennsylvania, Philadelphia, PA, USA
The incidence of obesity-related nephropathy (ORG) is increasing with the growing incidence of obesity. ORG is associated with morbid obesity, proteinuria and renal biopsy findings of focal global and segmental glomerulosclerosis (FSGS), which can be associated with significant renal impairment. Weight reduction is associated with improvement of ORG, however, conservative measures aiming at long-term weight reduction are difficult to achieve. Bariatric surgery is the most effective way of achieving long-term weight reduction. We present a case of ORG with nephrotic-range proteinuria and FSGS on renal biopsy. Following bariatric surgery, patient achieved successful weight reduction with significant decrease in proteinuria and stabilization of renal function.Correspondence to:
D.L. Cohen, MD; University of Pennsylvania, Renal and Pathology Divisions, 210 White Building, 3400 Spruce Street, Philadelphia, PA 19104, USA
Email: cohendl@mail.med.upenn.edu

Abstract

N. Miura, R. Aoyama, W. Kitagawa, H. Yamada, K. Nishikawa and H. Imai

Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Aichi, Japan
A 59-year-old woman with ulcerative colitis developed red eyes, pleural effusion, eosinophilia and urinary abnormalities after restarting of sulphasalazine treatment. Light microscopy of a kidney biopsy revealed segmental necrotizing glomerulonephritis without deposition of immunoglobulin or complement. Proteinase 3-antineutrophil cytoplasmic antibody (PR3-ANCA) titer was elevated at 183 ELISA units (EU) in sera (normal range less than 10 EU), myeloperoxidase-ANCA was negative. PR3-ANCA titer was 250 and 1,070 EU in pleural effusions on right and left side, respectively. Although cessation of sulphasalazine treatment resulted in improvements in fever, red eyes, chest pain, titer of C-reactive protein and volume of the pleural effusions, we initiated steroid therapy, because PR3-ANCA titer rose to 320 EU, eosinophil count increased to 1,100 cells/µl, and the pleural effusion remained. One month after steroid therapy, the pleural effusion disappeared, and PR3-ANCA titer normalized 3 months later. This case suggests that sulphasalazine can induce PR3-ANCA-positive necrotizing glomerulonephritis.Correspondence to:
H. Imai, Prof. and Chairman; Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute-cyo, Aichi, 480-1195, Japan
Email: imaihiro@aichi-med-u.ac.jp

Abstract

K. Lhotta¹,², A. Gehringer³, P. Jennings⁴, F. Kronenberg³, C. Brezinka⁵, I. Andersone⁶ and V. Strazdins⁶

¹Department of Nephrology and Dialysis, Academic Teaching Hospital Feldkirch, ²Division of Clinical Nephrology, ³Department of Medical Genetics, Division of Genetic Epidemiology, Molecular and Clinical Pharmacology, ⁴Division of Physiology, Department of Physiology and Medical Physics, ⁵Department of Obstetrics and Gynecology, Innsbruck Medical University Innsbruck, Austria and ⁶Department of Nephrology, University Hospital for Children, Riga, Latvia
Background: Familial juvenile hyperuricemic nephropathy (FJHN) is a rare autosomal dominant disease caused by mutations in the uromodulin gene (UMOD) and leading to gout, tubulointerstitial nephropathy and end-stage renal disease. Case reports and results: A Latvian family suffering from FJHN is described. The father of the family developed ESRD at age 36. His daughter was diagnosed with gout and chronic kidney disease at age 14 years. A renal biopsy revealed tubulointerstitial disease; 2 sons were diagnosed at age 9 and 4 with elevated uric acid levels and reduced fractional uric acid excretion. Urinary uromodulin was normal in the younger boy, but markedly decreased in the 2 other patients. Genetic analysis revealed a previously undescribed D196Y mutation in the UMOD gene. The female patient became pregnant at age 23. During pregnancy serum creatinine decreased from 2.0 to 1.5 mg/dl and blood pressure remained low. Analysis of the baby’s umbilical cord blood and a mouth swab showed the presence of the D196Y mutation. Its urinary uromodulin excretion was in the low normal range. Conclusion: The uromodulin excretion pattern observed in the investigated family suggests that urinary uromodulin decreases in FJHN from low normal values at childhood to extremely low levels in early adulthood. In addition, this first report on pregnancy in a patient with FJHN shows normal adaptation despite markedly reduced renal function.Correspondence to:
Dr. K. Lhotta; Department of Nephrology and Dialysis, Academic Teaching Hospital Feldkirch, Carinagasse 47, 6800 Feldkirch, Austria
Email: Karl.Lhotta@lkhf.at

Abstract

S.H. Kwon¹,², H.C. Cho¹,², S.W. Lee¹,², D.Y. Kim¹,², W.C. Joo¹,², W.H. Lee³, J.H. Song¹,² and M.-J. Kim¹,²

¹Division of Nephrology and Hypertension, ²Kidney Disease Research Groupand ³Division of Cardiology, Department of Internal Medicine, Inha University College of Medicine, Incheon, Republic of Korea
Of the several complications known to develop after cardiac catheterization, simultaneous acute renal infarction and renal subcapsular hematoma is rare. Here, the authors report a case of acute renal infarction with subcapsular hematoma that developed 4 hours after cardiac catheterization.Correspondence to:
M.-J. Kim, MD; Kidney Center, Inha University Hospital, 7-206, 3-Ga, Sinhung-Dong, Jung-Gu, Incheon, Republic of Korea

Email: nhkimj@inha.ac.kr

Abstract

M. Eriguchi, T. Nagao, T. Kamimura, K. Sugawara, K. Mitsuiki and A. Harada

Kidney Center, Matsuyama Red Cross Hospital, Matsuyama City, Japan
In this report, we describe a patient who contracted fatal cryptococcosis after the induction of hemodialysis. A 76-year-old man was hospitalized to initiate hemodialysis. On admission, clinical findings showed no signs of any infections, and hemodialysis was inducted favorably. On the 6th hospital day he suddenly had a dyspnea and died from acute respiratory failure having a dyspnea for only 6 h. By microscopic examination at autopsy, we detected microemboli in the pulmonary capillary arteries caused by Cryptococcus and that the embolic source was a multiple-abscessed spleen. To the best of our knowledge, this is the first reported case of pulmonary capillary microembolism caused by cryptococcemia.Correspondence to:
M. Eriguchi; Bunkyo-cho 1, Matsuyama City, Ehime prefecture, 790-8524, Japan
Email: masahiro@matsuyama.jrc.or.jp

Abstract

C.H. Chang, J.Y. Huang, P.C. Lai and C.W. Yang

Department of Nephrology, Chang Gung Memorial Hospital, Linkou Medical Center, School of Medicine, Chang Gung University, Taiwan (R.O.C.)
Mediastinal abscess is a rare but life-threatening disease with grave prognosis if not recognized in time. The diagnosis of this entity is hampered by its nonspecific presentation. Thus, a high index of clinical suspicion is one of the keystones in the successful management of these patients. Currently, mediastinitis occurred mostly as a complication post cardiovascular or thoracic surgical procedures. Rarely, primary mediastinitis developed as a result of hematogenous spread. We report the case of primary mediastinitis in a renal failure patient who had Staphylococcus aureus bacteremia. Despite antibiotic treatment, she had massive hemoptysis and eventually succumbed to the disease. To our knowledge, this is the first report of Staphylococcus aureus bacteremia complicating mediastinal abscess in a dialysis patient with a native arteriovenous shunt. Our experience in this case suggests that dialysis patients are under constant risk of staphylococcal infection due to regular venous puncture. Measures should be taken to reduce the risk and staphylococcal infection should not be forgotten in any dialysis patient with fever of unknown origin.Correspondence to:
Dr. P.C. Lai, MD, PhD; Kidney Institute, Chang Gung Memorial Hospital, Linkou Medical Center, Taiwan
Email: georgep.lai@gmail.com

Abstract

C.-L. Lang¹,³, C.-K. Chiang¹,², K.-Y. Hung¹ and K.-D. Wu¹

¹Department of Internal Medicine, ²Department of Diagnostics and Therapeutics, School of Medicine, National Taiwan University, ³Department of Internal Medicine, Cardinal Tien Hospital, Yung Ho Branch, Taiwan
Gram-negative pathogen-induced continuous ambulatory peritoneal dialysis- (CAPD) related peritonitis is increasing, especially that caused by enteric pathogens. We describe a 54-year-old Taiwanese man with a case of Campylobacter jejuni-mediated CAPD-related peritonitis and bacteremia. Positive Campylobacter jejuni dialysate and blood cultures confirmed the diagnosis of CAPD-mediated systemic infection. We initially administered intraperitoneal ceftazidime, amikacin and oral azithromycin, but the patient did not recover. We then administered i.v. ciprofloxacin and replaced the hemodialysis (HD). The patient recovered and was discharged with maintenance HD. Treatment of Campylobacter jejuni-mediated CAPD peritonitis is a challenge in areas with high antibiotic resistance.Correspondence to:
C.-K. Chiang MD, PhD; Department of Internal Medicine, National Taiwan University Hospital, No.7 Chung-Shan South Road, Taipei, Taiwan
Email: ckchiang@ntu.edu.tw; ckchiang@ntuh.gov.tw

Abstract

E.E. Politis, J. Droulias, N. Nikolopoulou, V. Hadjiconstantinou and T. Apostolou

Abstract

S. Unver, E.M. Atasoyu, H. Uluutku, I. Sucullu, S. Yildirim and T.R. Evrenkaya

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Volume 71, No. 1/2009(January)